Abstract:

Abstract The kidney has a strong compensatory ability, after acute kidney injury even if the serum creatinine returned to baseline, but the renal structure has not been fully restored. AKI can lead to tissue incomplete repair, resulting in the injury of vascular endothelial cells, microvascular reduce, ischemia and hypoxia leads to hyperplasia of fibrous tissue and renal fibrosis. AKI increase the risk of occurrence of CKD and ESRD. In addition, the chronic dysregulation of these factors (such as hypoxia inducible factor, vascular endothelial growth factor, transforming growth factor beta 1) over time and their net interactions are likely to determine the extent of fibrotic responses and organ function, eventually leading to the occurrence of chronic kidney disease

Key words: Acute kidney injury, Chronic kidney disease, Pathophysiology, Molecular mechanism